DNA damage responses to oxidative stress

Barzilai, Ari; Yamamoto, Ken-Ichi

doi:10.1016/j.dnarep.2004.03.002

Cited by 796DNA Repair MechanismsRedox biology and oxidative stressEffects of Radiation Exposure

DNA damage responses to oxidative stress

Barzilai, Ari, Yamamoto, Ken-Ichi·2004·DNA Repair

DOI 10.1016/j.dnarep.2004.03.002

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Abstract

The DNA damage response is a hierarchical process. DNA damage is detected by sensor proteins such as the MRN complex that transmit the information to transducer proteins such as ATM and ATR, which control the damage response through the phosphorylation of effector proteins. The extent of the DNA damage determines cell fate: cell cycle arrest and DNA repair or the activation of apoptotic pathways. In aerobic cells, reactive oxygen species (ROS) are generated as a by-product of normal mitochondrial activity. If not properly controlled, ROS can cause severe damage to cellular macromolecules, especially the DNA. We describe here some of the cellular responses to alterations in the cellular redox state during hypoxia or oxidative stress. Oxidative damage in DNA is repaired primarily via the base excision repair (BER) pathway which appears to be the simplest of the three excision repair pathways. To allow time for DNA repair, the cells activate their cell cycle checkpoints, leading to cell cycle arrest and preventing the replication of damage and defective DNA.

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Cells use multiple DNA repair and DNA damage response pathways to preserve genomic integrity after oxidative DNA damage.
“In response to oxidative DNA damage, various DNA repair and DNA damage response (DDR) pathways are employed by cells to maintain genomic integrity [12, 18, 19, 31]”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [12]

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Authors: Barzilai, A., & Yamamoto, K.-I.
Affiliations: Tel Aviv University (IL)
Kanazawa University (JP)
Corresponding author: Barzilai, Ari
ORCID: Barzilai, Ari
Yamamoto, Ken-Ichi
Venue: DNA Repair
Publisher: Elsevier BV
Published: 2004-08
Volume: 3
Issue: 8-9
Pages: 1109-1115
ISSN: 1568-7856 (ISSN-L)
1568-7864
DOI: 10.1016/j.dnarep.2004.03.002
OpenAlex: W2035396914
Cited by: 796
References: 75
Citations by year: 2026: 19 · 2025: 51 · 2024: 42 · 2023: 41 · 2022: 58 · 2021: 41 · 2020: 43 · 2019: 50 · 2018: 52 · 2017: 40 · 2016: 33 · 2015: 36 · 2014: 40 · 2013: 34 · 2012: 36
FWCI: 1.98
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: DNA repair (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
Keywords: DNA damage response, oxidative stress, reactive oxygen species, MRN complex, ATM, ATR, protein phosphorylation, cell cycle checkpoints, cell cycle arrest, apoptosis, base excision repair, hypoxia, redox state, mitochondrial reactive oxygen species
MeSH terms: Animals, Hypoxia, Cell Cycle, DNA Damage, DNA Repair, Humans, Mitochondria, Oxidation-Reduction, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Cell Lineage

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